Objective To study the effects of schisandrin B (Sch B) on the apoptosis of human breast cancer MDA-MB-231 cells and its mechanism. Methods Cell counting reagent (CCK-8) was used to detect the effect of Sch B on the survival rate of MDA-MB-231 cells. MDA-MB-231 cells were treated with Sch B (10, 20, 40 μmol/L) for 24 hours. The cell death was detected by Annexin V-FITC/PI. The levels of intracellular reactive oxygen species (ROS) were detected by DCFA-DA fluorescent probe. Apoptosis and the expression of endoplasmic reticulum stress related proteins (Bcl-2、Bax、CHOP、GPR78、PERK、p-PERK、p-eIF2α、eIF2) were detected by Western blot. Results Compared with the blank group, the cell survival rate decreased significantly (P<0.01) with the increase of Sch B concentration, and its IC₅₀ was 19.16 μmol/L. Compared with the control group, Sch B groups (10, 20, 40 μmol/L) inhibited cell clone formation in a dose-dependent manner (P<0.05). Sch B groups (10, 20, 40 μmol/L) induced apoptosis (P<0.05), significantly reduced the expression of anti-apoptotic protein Bcl-2 and significantly increased the expression of pro-apoptotic protein Bax (P<0.05). Sch B groups (10, 20, 40 μmol/L) significantly increased the level of intracellular ROS in a dose-dependent manner (P<0.05). Sch B groups (10, 20, 40 μmol/L) stimulated endoplasmic reticulum stress and increased the expressions of endoplasmic reticulum stress-related proteins CHOP, GPR78 and p-eIF2α in a dose-dependent manner (P<0.05). Conclusion Sch B induces apoptosis of MDA-MB-231 cells through ROS mediated endoplasmic reticulum stress.

Betulinic acid (BA), a pentacyclic lupane-type triterpene, has a wide range of bioactivities. The main objective of this work was to evaluate the hepatoprotective activity of BA and the potential mechanism underlying the ability of this compound to prevent liver damage induced by alcohol in vivo. Mice were given oral doses of BA (0.25, 0.5, and 1.0 mg/kg) daily for 14 days, and induced liver injury by feeding 50% alcohol orally at the dosage of 10 ml/kg after 1 h last administration of BA. BA pretreatment significantly reduced the serum levels of alanine transaminase, aspartate transaminase, total cholesterol, and triacylglycerides in a dose-dependent manner in the mice administered alcohol. Hepatic levels of glutathione, superoxide dismutase, glutathione peroxidase, and catalase were remarkably increased, while malondialdehyde contents and microvesicular steatosis in the liver were decreased by BA in a dose-dependent manner after alcohol-induced liver injury. These findings suggest that the mechanism underlying the hepatoprotective effects of BA might be due to increased antioxidant capacity, mainly through improvement of the tissue redox system, maintenance of the antioxidant system, and decreased lipid peroxidation in the liver.
Animals ; Antioxidants/pharmacology ; Blood Chemical Analysis ; Enzymes/blood ; Ethanol/*toxicity ; Lipid Peroxidation/drug effects ; Liver/*drug effects/enzymology/metabolism/pathology ; Male ; Mice ; Random Allocation ; Triterpenes/*pharmacology